Abstract

The study had two main purposes: (1) to determine whether the foveal visual sensitivities of people treated for high blood pressure (vascular hypertension) differ from the sensitivities of people who have not been diagnosed with high blood pressure and (2) to understand how visual adaptation is related to standard measures of systemic cardiovascular function. Two groups of middle-aged subjects—hypertensive and normotensive—were examined with a series of test/background stimulus combinations. All subjects met rigorous inclusion criteria for excellent ocular health. Although the visual sensitivities of the two subject groups overlapped extensively, the age-related rate of sensitivity loss was, for some measures, greater for the hypertensive subjects, possibly because of adaptation differences between the two groups. Overall, the degree of steady-state sensitivity loss resulting from an increase of background illuminance (for 580-nm backgrounds) was slightly less for the hypertensive subjects. Among normotensive subjects, the ability of a bright (3.8-log-td), long-wavelength (640-nm) adapting background to selectively suppress the flicker response of long-wavelength-sensitive (LWS) cones was related inversely to the ratio of mean arterial blood pressure to heart rate. The degree of selective suppression was also related to heart rate alone, and there was evidence that short-term changes of cardiovascular response were important. The results suggest that (1) vascular hypertension, or possibly its treatment, subtly affects visual function even in the absence of eye disease and (2) changes in blood flow affect retinal light-adaptation processes involved in the selective suppression of the flicker response from LWS cones caused by bright, long-wavelength backgrounds.

For each of the three types of hypertensive retinopathy characteristics—vascular sclerosis, focal arteriolar constriction, and arteriovenous narrowing—grades were assigned on a five-point scale. For each characteristic, a score of 0 signified that the vasculature was indistinguishable from that of a young healthy person, a score of 1 signified a minimal difference, a score of 2 signified a more marked difference, and a score of 3 signified more difference yet, by itself enough to indicate a high probability of past or present vascular disease. No person tested had a score of 4, and two people were excluded from the study on the basis of sclerosis scores of 3. The distributions of scores for each subject group are given next. The numbers in parentheses refer to the number of subjects assigned a score of 0, 1, or 2, respectively. Focal arteriolar constriction: normotensive subjects (22, 5, 2), hypertensive subjects (22, 4, 1), and tamoxifen subjects (25, 5, 0). Arteriovenous narrowing: normotensive subjects (20, 7, 2), hypertensive subjects (21, 4, 2), and tamoxifen subjects (24, 6, 0). Vascular sclerosis: normotensive subjects (12, 12, 4), hypertensive subjects (15, 9, 3), and tamoxifen subjects (15, 15, 0).

The specific order of testing depended on many considerations, some of which are specified in the text. The 1.6-log-td, 580-nm background preceded the 3.6-log-td, 580-nm background so that the dynamics of recovery of SWS-cone-mediated sensitivity could be assessed after a sudden large increase of background illuminance.40(The dynamics of recovery were affected by tamoxifen.35) The use of a 2.0-log-td, 580-nm background was based on preliminary results that suggested that the crossover points of an MWS–LWS-cone mechanism and an SWS-cone mechanism might differ between the hypertensive and the normotensive subject groups. (This suggestion was not verified on prospective testing.) The 2.0-log-td background preceded all other backgrounds by default, given all the other constraints. The 2.6-log-td, 580-nm background was used in order to assess the effects of background illuminance on flicker sensitivity under conditions in which departures from Weber’s law would not be great. There were several practical reasons for merging the protocols for two investigations (one concerning cardiovascular function and the other concerning effects of tamoxifen). Many of the same subjects served as controls for each investigation, and a second nonhypertensive subject group (the tamoxifen subjects) was used prospectively to confirm and to interpret effects from the normotensive subject group.

All the variables listed in Table 1were used in conducting a factor analysis for the normotensive subjects’ data. The number of factors was chosen a priorito be four, and a Varimax rotation was used. The first three factors were readily identified as (1) an SWS-cone-sensitivity factor, (2) a flicker-sensitivity factor, and (3) a factor that reflected sensitivities mainly for test wavelengths ranging from approximately 500 to 560 nm on the 2.0-log-td, 580-nm background. The fourth factor was less well defined but reflected sensitivities mainly on the 3.6-log-td, 580-nm background. Because the normotensive group’s maximal sensitivity in the 500- to 580-nm range occurred at 540 nm for the 2.0-log-td, 580-nm background, factor 3 can be identified with an MWS–LWS cone mechanism. Sensitivity to a 580-nm test on the 2.0-log-td 580-nm background was represented approximately equally in factors 2 and 3, and it was the only non-flicker-sensitivity variable with appreciable representation in factor 2.

The threshold elevation from a 2.0- to a 3.6-log-td background did not appear to differ between groups for an SWS-cone mechanism (p=0.380for 440-nm tests), but it may have differed for an MWS–LWS cone mechanism (p= 0.050for 560-nm tests).

The rank order correlations between MAP/HR and logfl. sens.580-logfl. sens.640were computed for the 2.6- and for the 3.6-log-td 580-nm backgrounds. For the normotensive subjects, these rank-order correlations were, respectively, Spearman r=-0.19and Spearman r=0.14.For the high-blood-pressure subjects, the rank-order correlations were, respectively, Spearman r=-0.03and Spearman r=-0.11.

Adding age to the regression equation for ΔFSλ would not have improved the fit of the regression line to the data; the overall correlation would have changed from R=0.57to R=0.58.Nor was age itself correlated with ΔFSλ (Spearman r=-0.09).Age may have been weakly correlated with MAP2/HR2(Spearman r=0.30,p=0.18).

For the normotensive subjects, the regression equation was ΔFSλ=1.20-0.40(MAP2/HR2)+0.29 ΔT.For the tamoxifen subjects, the regression equation was ΔFSλ= 0.96-0.24(MAP2/HR2)+0.29 ΔT.

The rank order correlation between MAP2/HR2and ΔT was Spearman r=-0.02for the normotensive subjects and Spearman r=-0.12for the tamoxifen subjects.

The correlation between an increase of heart rate and a reduction of mean deviation would have remained significant if the data from subjects who were administered 30-2 visual fields were excluded from the calculation.

It is possible that the regression model could have been refined still further. When the normotensive subjects were classified by the presence or absence of arteriovenous narrowing, and this categorical factor was added to the three quantitative factors (MAP2/HR2,ΔT, and Δ(MAP/HR), all four factors were significant in an analysis of covariance (p=0.001,p=0.003,p=0.016,and p=0.021,respectively). Arteriovenous narrowing was associated with more selective suppression of the response from LWS cones.

Visual Neurosci

Other

For each of the three types of hypertensive retinopathy characteristics—vascular sclerosis, focal arteriolar constriction, and arteriovenous narrowing—grades were assigned on a five-point scale. For each characteristic, a score of 0 signified that the vasculature was indistinguishable from that of a young healthy person, a score of 1 signified a minimal difference, a score of 2 signified a more marked difference, and a score of 3 signified more difference yet, by itself enough to indicate a high probability of past or present vascular disease. No person tested had a score of 4, and two people were excluded from the study on the basis of sclerosis scores of 3. The distributions of scores for each subject group are given next. The numbers in parentheses refer to the number of subjects assigned a score of 0, 1, or 2, respectively. Focal arteriolar constriction: normotensive subjects (22, 5, 2), hypertensive subjects (22, 4, 1), and tamoxifen subjects (25, 5, 0). Arteriovenous narrowing: normotensive subjects (20, 7, 2), hypertensive subjects (21, 4, 2), and tamoxifen subjects (24, 6, 0). Vascular sclerosis: normotensive subjects (12, 12, 4), hypertensive subjects (15, 9, 3), and tamoxifen subjects (15, 15, 0).

The specific order of testing depended on many considerations, some of which are specified in the text. The 1.6-log-td, 580-nm background preceded the 3.6-log-td, 580-nm background so that the dynamics of recovery of SWS-cone-mediated sensitivity could be assessed after a sudden large increase of background illuminance.40(The dynamics of recovery were affected by tamoxifen.35) The use of a 2.0-log-td, 580-nm background was based on preliminary results that suggested that the crossover points of an MWS–LWS-cone mechanism and an SWS-cone mechanism might differ between the hypertensive and the normotensive subject groups. (This suggestion was not verified on prospective testing.) The 2.0-log-td background preceded all other backgrounds by default, given all the other constraints. The 2.6-log-td, 580-nm background was used in order to assess the effects of background illuminance on flicker sensitivity under conditions in which departures from Weber’s law would not be great. There were several practical reasons for merging the protocols for two investigations (one concerning cardiovascular function and the other concerning effects of tamoxifen). Many of the same subjects served as controls for each investigation, and a second nonhypertensive subject group (the tamoxifen subjects) was used prospectively to confirm and to interpret effects from the normotensive subject group.

Adding age to the regression equation for ΔFSλ would not have improved the fit of the regression line to the data; the overall correlation would have changed from R=0.57to R=0.58.Nor was age itself correlated with ΔFSλ (Spearman r=-0.09).Age may have been weakly correlated with MAP2/HR2(Spearman r=0.30,p=0.18).

For the normotensive subjects, the regression equation was ΔFSλ=1.20-0.40(MAP2/HR2)+0.29 ΔT.For the tamoxifen subjects, the regression equation was ΔFSλ= 0.96-0.24(MAP2/HR2)+0.29 ΔT.

The rank order correlation between MAP2/HR2and ΔT was Spearman r=-0.02for the normotensive subjects and Spearman r=-0.12for the tamoxifen subjects.

The correlation between an increase of heart rate and a reduction of mean deviation would have remained significant if the data from subjects who were administered 30-2 visual fields were excluded from the calculation.

It is possible that the regression model could have been refined still further. When the normotensive subjects were classified by the presence or absence of arteriovenous narrowing, and this categorical factor was added to the three quantitative factors (MAP2/HR2,ΔT, and Δ(MAP/HR), all four factors were significant in an analysis of covariance (p=0.001,p=0.003,p=0.016,and p=0.021,respectively). Arteriovenous narrowing was associated with more selective suppression of the response from LWS cones.

All the variables listed in Table 1were used in conducting a factor analysis for the normotensive subjects’ data. The number of factors was chosen a priorito be four, and a Varimax rotation was used. The first three factors were readily identified as (1) an SWS-cone-sensitivity factor, (2) a flicker-sensitivity factor, and (3) a factor that reflected sensitivities mainly for test wavelengths ranging from approximately 500 to 560 nm on the 2.0-log-td, 580-nm background. The fourth factor was less well defined but reflected sensitivities mainly on the 3.6-log-td, 580-nm background. Because the normotensive group’s maximal sensitivity in the 500- to 580-nm range occurred at 540 nm for the 2.0-log-td, 580-nm background, factor 3 can be identified with an MWS–LWS cone mechanism. Sensitivity to a 580-nm test on the 2.0-log-td 580-nm background was represented approximately equally in factors 2 and 3, and it was the only non-flicker-sensitivity variable with appreciable representation in factor 2.

The threshold elevation from a 2.0- to a 3.6-log-td background did not appear to differ between groups for an SWS-cone mechanism (p=0.380for 440-nm tests), but it may have differed for an MWS–LWS cone mechanism (p= 0.050for 560-nm tests).

The rank order correlations between MAP/HR and logfl. sens.580-logfl. sens.640were computed for the 2.6- and for the 3.6-log-td 580-nm backgrounds. For the normotensive subjects, these rank-order correlations were, respectively, Spearman r=-0.19and Spearman r=0.14.For the high-blood-pressure subjects, the rank-order correlations were, respectively, Spearman r=-0.03and Spearman r=-0.11.

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